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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obesity is associated with absolute and relative expansion of the extracellular water compartment (ECW). The effects of substantial and prolonged weight reduction on body water distribution are unknown, however. The authors studied total body water (TBW) by tritiated water dilution, ECW by 35SO4 dilution, exchangeable sodium (Na(e)) by 24Na, and total body potassium (TBK) by 40K whole-body counting in 25 severely obese women (body mass index [BMI] = 48 +/- 7 kg.m-2, mean +/- standard deviation) aged 36 +/- 8 years before and at intervals after gastric restrictive (GR; n = 12) and malabsorptive (MA; n = 13) operations for obesity. Results are compared with a control group of 26 healthy normal-weight women (BMI = 21 +/- 2). Before operation, the obese patients had absolute elevations of all water compartments compared with controls, with significantly higher ratios of Na(e) to TBK (1.17 +/- 0.13 versus 0.91 +/- 0.10; p less than 0.05) and ECW to intracellular water (ICW) (E/I = 0.82 +/- 0.17 versus 0.63 +/- 0.06; p less than 0.05). After weight loss of 52 +/- 20 kg in MA and 47 +/- 19 kg in GR patients (nonsignificant between groups) to a stable level 22 +/- 8 months after operation, there were statistically significant reductions in TBW, ICW, TBK, and Na(e) in both groups, but a significant reduction in ECW only after GR. Adjusting for preoperative weight, duration of follow-up, and rate of weight loss, E/I was greater after MA than GR (1.09 +/- 0.25 versus 0.82 +/- 0.14; p less than 0.05). The elevated preoperative E/I ratio did not normalize with weight loss after surgery, and the response was related to the type of operation. The finding remains to be explained although the increased E/I after MA may reflect mild protein-calorie malnutrition not detectable in the blood. The persistence of elevated E/I with significant weight loss after GR might imply an intrinsic or irreversible imbalance of fluid distribution in obese patients.
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PMID:Body composition and surgical treatment of obesity. Effects of weight loss on fluid distribution. 163 4

The ability to identify the hypertensive patient who is destined to suffer a morbid or fatal complication in the long presymptomatic phase of this condition, when its natural history would be most subject to amelioration, is limited by the weak relation between the level of blood pressure and the occurrence of complications. Recent research indicates that the level of left ventricular (LV) mass--most conveniently measured by echocardiography--reflects the combined effects of a variety of factors involved in the pathophysiology of hypertension, including obesity, exaggerated blood pressure responses to everyday activity, high sodium intake and blood viscosity, and genetic factors predisposing to hypertension. Prospective studies indicate that LV mass is a stronger predictor of subsequent morbid events and death than blood pressure or other conventional risk factors except age. Preliminary findings of close relations between LV mass and arterial disease and between the change in LV mass during antihypertensive treatment and subsequent events contribute to explaining the strong predictive value of LV mass. Further research is needed to clarify the biologic basis of these observations and to determine whether stratification of hypertensive patients based on their level of LV mass can improve the treatment of hypertension.
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PMID:Left ventricular mass as a measure of preclinical hypertensive disease. 163 38

This study was initiated to elucidate the mechanisms behind valproate-induced weight gain. Eight patients with epilepsy were studied with identical examination programs before and during the end of the first month of treatment with sodium valproate (VPA). The measurements included registration of food intake, indirect calorimetry, and determination of pancreatic and thyroid hormones, catecholamines, albumin, electrolytes, glycerol, and free fatty acids. Measurements were performed both at the basal condition and during a 3-hour oral glucose tolerance test (OGTT). After the start of VPA treatment, the mean levels during the OGTT of plasma glucose and catecholamines were significantly decreased by 7% and 25%, respectively (P less than .05). The mean ratio of insulin to glucagon decreased by 37% (P less than .01). During the glucose load, the decreases in free fatty acids were less pronounced after the start of VPA treatment, whereas the mean levels of glycerol were found to be unchanged. We detected no differences between the two periods with regard to total energy intake or macronutrient selection, energy expenditure, or thyroid hormones. As VPA is known to affect the concentration of carnitine in humans, it is hypothesized that a possible VPA-induced deficiency of the beta-oxidation of fatty acids is important for the development of obesity in epileptic patients in long-term treatment with VPA, but changes in catecholamines or other hormones might also be of importance.
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PMID:Metabolic changes during treatment with valproate in humans: implication for untoward weight gain. 164 Aug 53

This article details the development, delivery, and evaluation of a six-session nutrition course entitled "Eating Today for a Healthier Tomorrow." The course addressed nutrition practices associated with the reduction of risk for coronary heart disease, cancer, osteoporosis, and obesity. Teaching teams, consisting of an extension agent and a registered dietitian, were used in course delivery. A wide variety of printed and audiovisual teaching aids helped participants learn through discussion, goal setting, games, and food tasting. Evaluation components of the course included demographic and pre- and post-course food frequency information as well as an overall evaluation by each participant. Post-course evaluation data were collected at a reunion session held 2 months after course completion. One hundred forty-two of 195 participants (73%) completed the course and the evaluation. Three-fourths of the participants had a family history of at least one of the life-style diseases addressed by the course. The food frequency results indicated that participants made some significant changes in their food practices. They decreased the number of times they selected high-fat cheese, regular red meats, foods from the saturated fatty acid group, desserts, sodium-rich products, and tea/coffee (p less than .05), and they increased selection of low-fat dairy products (p less than .05). Further study is recommended to determine whether individuals maintain the dietary changes and how those changes affect others in the person's immediate environment.
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PMID:A risk-reduction nutrition course for adults. 168 28

Data from 49 men and 48 women included in the Cardiovascular Diseases and Alimentary Comparison (CARDIAC) Study in Perth, Western Australia, were analyzed. Systolic blood pressure (SBP) and diastolic blood pressure (DBP) were positively correlated (p less than 0.01) with urine sodium, creatine, taurine, histidine, and 3-methyl histidine but not with calcium, magnesium, or potassium. SBP was related (p less than 0.01) with body mass index (BMI). Urine nitrogen, creatinine, and amino acids correlated (p less than 0.001) with each other and with urine sodium, potassium, calcium, and magnesium. Urine magnesium correlated (p less than 0.001) with urine calcium and potassium; urine calcium was not related significantly to urine sodium or potassium. In backwards multiple regression with data from urine collections, SBP was significantly related only to urine sodium (11.9% of variance explained). If alcohol was included as an independent variable, reducing the number of valid cases because of missing values, both alcohol and urine sodium were significant in regression (19.9% of variance explained). In men, DBP was significantly related to BMI and the ratio of 3-methylhistidine to creatine (23.7% of variance explained). For DBP in women, urine sodium was the only variable needed in regression (58.4% of variance explained). Interpretation must be cautious, because these analyses are based on relatively few cases and on single 24-h urine samples. The data are in keeping with suggestions that obesity, alcohol consumption, a meat diet, and sodium intake are important factors predisposing to elevation of blood pressure.
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PMID:Cardiovascular Diseases and Alimentary Comparison Study: preliminary analysis of data from Western Australia. 170 20

Hyperinsulinemia and insulin resistance have been postulated to link obesity and hypertension. Evidence supporting this concept derives mainly from epidemiological studies showing a correlation between insulin resistance, hyperinsulinemia, and blood pressure and from short-term studies suggesting that insulin has renal and cardiovascular actions that, if sustained, could elevate blood pressure. However, a cause-and-effect relation between insulin and hypertension has not been clearly established. Recent studies indicate that chronic hyperinsulinemia, similar to that found in obese hypertensive patients, did not raise blood pressure in normal dogs, even when renal excretory capability was reduced by prior removal of kidney mass. Chronic insulin infusion also failed to elevate blood pressure in dogs maintained on a high sodium intake and did not potentiate the long-term blood pressure responses to angiotensin II or norepinephrine. The presence or absence of insulin resistance may not be a major factor in determining the blood pressure response to hyperinsulinemia since chronic insulin infusion also failed to cause hypertension in obese, insulin-resistant dogs. Although hyperinsulinemia causes transient sodium retention, sustained decreases in renal excretory capability sufficient to cause chronic hypertension did not occur in dogs. In rats, insulin infusion causes small increases in blood pressure, although several characteristics of the hypertension (e.g., salt-sensitivity) differ from those observed in obese human hypertensive patients. Whether humans more closely resemble dogs or rats with respect to their long-term cardiovascular responses to insulin remains to be determined. However, very high insulin levels in humans with insulinoma do not cause hypertension, and several studies suggest that there is only a weak correlation between plasma insulin concentration and blood pressure in normal humans. Therefore, additional factors besides hyperinsulinemia per se may be responsible for a major component of obesity-associated hypertension.
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PMID:Obesity-associated hypertension. Hyperinsulinemia and renal mechanisms. 173 Apr 54

The purpose of this study was to determine whether genetically obese Zucker rats have higher arterial pressures than lean littermates on normal and high sodium intakes. Mean arterial pressure was directly measured in chronically instrumented Zucker rats (six lean [weight, 345.8 +/- 8.0 g] and five obese [529.0 +/- 6.2 g]) for 2 weeks on both a normal (2 meq sodium/day) and high (6 meq sodium/day) sodium intake (7 days each). In addition, daily heart rate, water intake, urine output, urinary sodium excretion, urinary potassium excretion, and weekly fasting plasma insulin levels were measured. Obese rats exhibited significantly lower heart rate and greater water intake and urine output compared with lean rats whether maintained on control or high sodium intakes. Urinary sodium excretion, however, was identical in lean and obese rats throughout the experiment. Fasting plasma insulin levels in obese rats were seven times greater than those in lean rats. When the rats were maintained on a 2 meq/day sodium intake, mean arterial pressures obtained from the two groups were similar: 103 +/- 1 versus 106 +/- 1 mm Hg (lean versus obese). An increase in sodium intake did not significantly affect mean arterial pressure in either group: 101 +/- 1 versus 105 +/- 1 mm Hg (lean versus obese). These results indicate that at 12-14 weeks of age, male obese Zucker rats do not exhibit higher resting arterial pressures than lean littermates when maintained on normal or high sodium intake.
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PMID:Obese Zucker rats are normotensive on normal and increased sodium intake. 173 Apr 61

Several studies support the premise that there is a strong relation between obesity and high blood pressure. Although the mechanism for obesity-related hypertension has not yet been fully elucidated, recent studies have suggested that abnormalities in renal sodium handling may be involved in the pathogenesis of obesity-induced hypertension. The purpose of the present study was to determine the effects of an acute saline load on renal excretory function in dogs with obesity-induced hypertension and in normotensive lean dogs. Experiments were performed in two groups of conscious, chronically instrumented dogs. One group of dogs (obese) was fed a high-fat diet for 5-6 weeks, and the other group (lean) ate a normal diet. The body weight of the obese dog group (26.3 +/- 0.7 kg) was 45% higher than the lean dog group (18.1 +/- 0.3 kg). Mean arterial pressure averaged 126 +/- 2 mm Hg in the obese dogs and 100 +/- 1 mm Hg in the lean dogs. The lean dogs had an average heart rate of 104 +/- 7 beats per minute, whereas the obese dogs averaged 134 +/- 8 beats per minute. Plasma renin activity was also significantly higher in the obese dogs. Both groups of dogs were given 135 meq sodium chloride over 60 minutes via an intravenous infusion of isotonic saline. Sodium and water excretion increased significantly in response to the acute saline load. However, the natriuresis and diuresis was markedly attenuated in the obese hypertensive dogs. During the first 40 minutes of saline loading, the increase in sodium and water excretion was 50-70% lower in the obese hypertensive dogs. The results of the present study indicate that obese hypertensive dogs have a reduced capability to excrete an acute sodium load. This abnormality in renal sodium handling may play a role in the pathogenesis of obesity-induced hypertension.
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PMID:Blunted natriuretic response to an acute sodium load in obese hypertensive dogs. 173 Apr 62

Twenty obese women aged 45-65 years with borderline hypertension were allocated randomly to either a group with an energy-restricted diet or to a control group. Body weight, blood pressure, urinary sodium, and urinary excretion of norepinephrine and plasma volume were recorded. Resting muscle sympathetic nerve activity was measured in the peroneal nerve by tungsten microelectrodes and expressed as bursts per minute. These measurements were repeated after 3 days of semistarvation and after a body weight reduction of 7% while each patient's weight was in a steady state. After 3 days of semistarvation, only body weight was reduced, whereas after the long-term energy intake restriction, there were reductions of body weight (79.9 +/- 3.4 versus 74.1 +/- 3.4 kg; p less than 0.001), diastolic blood pressure (93 +/- 3 versus 86 +/- 4 mm Hg; p = 0.01), and muscle sympathetic nerve activity (49 +/- 2 versus 42 +/- 3 bursts/min; p less than 0.05). Other variables were unchanged. There were no changes in body weight, blood pressure, or muscle sympathetic nerve activity in the control group. We conclude that body weight decrease in obesity results in a reduction of blood pressure that is at least partially caused by a reduction of sympathetic vasoconstrictor activity.
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PMID:Effect of energy-restricted diet on sympathetic muscle nerve activity in obese women. 174 59

Late diabetic effects are the sequelae of for a long time super elevated blood sugar levels. The diabetic nephropathy is the cause of the secondary arterial hypertension. The investigation seeks for the connections between the diabetes mellitus and the essential, that is primary hypertension. The two diseases frequently appear and clearly increase in the second half of life. Moreover, they are above average frequently associated with each other. Among brothers and sisters of diabetic hypertensives in comparison to normal cohorts clearly increased high blood pressure prevalences were found. The insulin resistance which could be proved in a great number of hypertensive and which has been known since more than two decades might be the connecting link between hypertension and diabetes mellitus. Like the obesity the essential hypertension can be associated with all degrees of an insulin hyposensitiveness. The sodium-retaining effect of the insulin might explain the increased sodium content of the body in hypertensives. The differential diagnostics of the essential hypertension should therefore seek for conditions of an insulin resistance. The type II diabetic lacks a release of bradykinin during muscle work. Thus the glucose uptake into the cell is unfavourable influenced and demands an increased insulin excretion. This genetically (?) fixed defect is found also in essential hypertensives. It could be the connecting link between the two diseases. ACE-inhibitors have via a kininase II inhibition an effect also on the bradykinin decomposition and can favourable influence the glucose uptake into the muscle. An improved insulin effect among the ACE-inhibitors was described. Therefore, they should be preferred in the treatment of hypertensive diabetics.
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PMID:[Diabetes mellitus and arterial hypertension. In search of the connecting link]. 177 26


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